Case reports

Dispatches After the introduction of routine childhood immunization against Haemophilus influenzae type b (Hib), the incidence of invasive Hib disease fell dramatically in several countries, including Australia (1-3). This decline has been most evident among children aged less than 5 years. Meanwhile , serious Hib infections, such as pneumonia and epiglottitis, have been increasingly recognized among elderly, debilitated, and immunosuppressed adults (4-6). However, clusters of Hib infection have rarely been reported in adults. To examine their relatedness, we investigated two fatal cases of Hib septicemia in a community nursing home. Case 1 In June 1996, a 71-year-old female nursing home resident was hospitalized after 3 days of unproductive cough, fevers, confusion, and increasing dyspnea. She had a history of cere-brovascular disease, muscular dystrophy, and congestive heart failure and was confined to a wheelchair. She had clinical signs of left lower lobe pneumonia and was afebrile. A blood film was normal, but a chest X-ray showed extensive bilateral pulmonary infiltrates. Arterial blood gases showed severe hypoxia in room air (PO 2 44 mm Hg, saturation 77%). Ceftriaxone 1 g and metronidazole 500 mg were given intravenously for suspected aspiration pneumonia, but the patient became severely hypotensive and died 8 hours after admission to the hospital. The following day, beta-lactamase-negative Hib was isolated from blood cultures collected before the patient died. Case 2 Two days after the first patient was hospitalized, an 80-year-old female resident of the same nursing home became ill with fever and sore throat. She had a history of chronic airflow limitation, mild renal impairment, and dementia. Her sore throat rapidly worsened, and the next day she was hospitalized with severe dysphagia. On examination, she was febrile (38.5 ° C) and hypotensive (90/60 mm Hg) and had pretracheal cellulitis. No clinical evidence of pneumonia was observed, and a chest X-ray was normal. She was intubated, and extensive epiglottitis, laryngitis, and tracheitis were noted. Ceftriaxone 2 g, genta-micin 80 mg, flucloxacillin 1 g, and metronidazole 500 mg were administered intravenously. Inotropes were given for hypotension and acute renal failure, but the patient's condition deteriorated rapidly, and she died 9 hours after admission to the hospital. Beta-lactamase-negative Hib was subsequently isolated from blood cultures collected before the patient died. Investigation For several months, these two women had occupied beds in the same six-bed room (the largest room) in the 44-bed nursing home. The home employed 37 nursing and ancillary staff. During …

The Leonard-Pritchard-Tibbits Prize of the University of Bristol requires lQt an undergraduate should " submit six case histories of surgical patients under his care during the term of his appointment as dresser with a brief c?>nmentary on each". The reports that follow are taken from the winning e$say for 1966-67; they form a commentary upon arterial surgery as seen by a Contemporary student?Editors. Case 1 . This is the case of a pensioner aged seventy-six years. She was first seen 111 the out-patients department by Mr. Peacock on the 15th July, 1965. She ^as then seventy-five years old. Her general practitioner had diagnosed an ^bdominal aortic aneurysm. On examination it was felt that she could stand having it resected. However, the patient was reluctant and in view of her age was not pressed to undergo the operation. The question of rupture was e*Plained to her. If ever she had much pain she would be gladly seen again. k Almost a year later the patient was admitted as an emergency at the Bristol Wal Infirmary. She had been seen by her doctor that morning with a three-?aV history of a great deal of pain in the abdomen. On examination he had ound her pale, her pulse was 100/min., regular and of fair volume, her B.P. "0/90 and her heart sounds I and II heard in all areas. There was a large Pulsating mass in the lumbar and umbilical regions of her abdomen and a lagnosis of a rupturing aneurysm was made. On admission to hospital she gave a history of a dull ache in the abdomen , nd back radiating down to the buttocks. This had lasted ten months and ad suddenly got worse three days previously. The pain was mild in the back nd spasmodic in the buttocks. She could only walk a distance of a hundred yards. There was no history of breathlessness or headaches. Previous medical history: Gastroenterostomy before 1955. Eczema treated cleared in 1955. Radical mastectomy for scirrhous carcinoma of the left reast in 1955. Early Dupuytren's contracture of both palms in 1962. examination: The patient was a small, frail looking lady with a pale ^ ^plexion. The hair was thin and fine. The hands, fingers and finger nails ere normal. Her temperature was 97.5?F. ? ^he pulse was 90 per minute, regular and of normal volume and form. ?th radial pulses were felt and were of equal volume. The jugular venous ]J~Ssure was not raised. The blood pressure was 190/90mm. mercury. On the J: chest was the scar of the radical mastectomy. The apex beat was not in h e but on palpation was localised to the fifth intercostal space, four , ches from the mid-sternal line. There was no thrill. The first and second art sounds were audible and normal in all areas. There were no murmurs or y adventitious sounds. The vessels of the fundi of the eyes were normal.
re&^n abdominal scar of a right paramedian incision was present. In the 6Jon of the umbilicus there was an oval swelling. This was found to be a pulsatile mass about four inches by six inches. It was tender to the touch and the pulsations were expansile.
Both the femoral pulses were of equal and good volume. The posterior tibial and dorsalis pedis arteries were palpable in both limbs and were of equal and good volume on both sides. The two carotids were palpable in the neck and were of equal volume. Both the lower limbs were warm and there was no difference in temperature between them.
Examination of the respiratory and nervous systems revealed no abnof' mality.
The diagnosis of a leaking aneurysm was made. She was sedated with ^ grain of omnopon intramuscularly.
Investigations: An x-ray of the chest on 7th May, 1966, showed some unfolding of the aorta with calcification. No lung lesion was seen.
An x-ray of the abdomen on the same date showed the intestinal gaS pattern to be normal. There was a line of calcification to the left of the lumbar spine which was in the wall of the abdominal aorta. The appearance was consistent with an aueurysm (Plate XXVII).
Liver function tests produced a total bilirubin of 0.2mg%; serum proteins on electrophoresis were within normal limits. The haemoglobin was 12.0G%' the packed cell volume 35%, the M.C.H.C. 34% and the E.S.R. 19mm.
hour. E.C.G. showed evidence of ischaemic heart disease.
On plain x-ray films of the urinary tract the renal outlines were within normal limits. The calcification in the wall of the abdominal aortic aneurysm was obvious. Degenerative changes were seen in the lumbar spine. On excrc tion urography no abnormality of the urinary tract was shown.
Blood urea and electrolyte levels were done. Urea was 26mg/100 plasma sodium 141mEq/litre, plasma potassium 3.8mEq/litre, plasma chlorioe 106mEq/litre, plasma bicarbonate 26.5mEq/litre, plasma protein 6.3%. . She remained quite comfortable during the first few days and slept wellbeing given 20 grains of dichloralphenazone every night.
On the 12th May she vomited and complained of abdominal pain. the 16th May she had back pain as well. It was decided that she should have her aneurysm explored with a view to resection and grafting. On the 17th the abdominal aortic aneurysm was explored by Mr. Terblanche. A long1' tudinal left paramedian incision was made. A resectable aneurysm was foufl^ in the aorta below the origin of the renal arteries and below the level of ^ left renal vein and extending up to the bifurcation and into the common itfaC arteries. During the early part of the anaesthetic, which was administered b) Professor Clutton-Brock, the patient developed a marked bundle-bran^ block. This necessitated the use of isoprenaline. Her general condition unsatisfactory and it was decided that she would not stand resection grafting of her aneurysm. Instead, however, the aneurysm was wired, using Peacock Stainless Steel Wiring machine inserting about two hundred feet ^ stainless steel wire from three sites (Plate XXVIII). Reconstitution of ^ anterior abdominal wall was performed in layers with nylon sutures, and sP was used for the skin.
Antibiotic therapy was begun with one mega-unit of penicillin and oi}? gram of streptomycin. This was continued with half a mega-unit of penicill"1 hourly and half a gram of streptomycin twelve hourly for seven days post-?Peratively. She was put into the intensive care unit and had to have constant supervision, and isoprenaline to treat her heart block. She subsequently returned to the ward and her further convalescence over the next few days ^as slow. She received intravenous fluids; one fifth normal dextrose saline, supplemented as necessary with potassium. Oral fluids were limited. However, she ^?ntinued to have very large quantities of gastric aspirate amounting on one day to almost three litres. An x-ray of the abdomen (supine and erect) on the 25th May displayed no Evidence of intestinal obstruction or ileus. A barium meal showed the stomach to be a little atonic and to contain a considerable amount of resting juice but lesion was seen in it or in the duodenum. Barium passed freely into the JeJUnum but no further. The aspiration tube had passed into the second part 5*the duodenum and had looped itself, so that the tip was still in the stomach.
Obstruction in the upper jejunum was suspected and it was decided to re-explore the abdomen. p On the 27th May, 1966, laparotomy was performed by Mr. Terblanche. r?fessor Clutton-Brock again administered the anaesthetic. There was no ^ardiac trouble this time. The obstruction was found to be at the site of her sastro-enterostomy efferent loop which had become kinked by adhesions to ^ aneurysm. The wall of the aneurysm had become fleshy and (edematous, Probably as a result of the wiring and subsequent thrombosis that had taken P^ce. The aneurysm at this stage was no longer pulsatile. j *ier subsequent post-operative course was satisfactory and there was no ^n8er any gastric aspirate. A slight urinary infection was cleared up with a ^?urse of sulphadimidine and she was eventually transferred to convalescence J1 the 20th June, 1966. She did have persistent lower back pain and a neuronic type of pain down the inner side of her left thigh, but this was much ^tter by the time of her discharge. at^ree wee^s later on the 11th July she was readmitted from convalescence Axbridge because of persistent diarrhoea, associated with poor appetite and ^asional vomiting. On examination she was dehydrated. Her tongue was v""| and her skin was lax. The pulse was 80 per minute, regular and of normal . Junie. The blood pressure was 120/90mm. Hg. There was no oedema, her gular venous pressure was not raised and her peripheral pulses were normal ^ equal on both sides. p scar of the operation was well healed. There was tenderness over the Ho tile aortic aneurysm especially in the left hypochondrium. There were s, ?ther masses and the bowel sounds were normal. Examination per rectum ?Wed soft greenish faeces but nothing else. Her respiratory and central hJV?Us systems revealed no abnormality. After she had been rehydrated her p ^oglobin was 12G%, her electrolytes were normal and her stool cultures gative. Bilirubin and serum proteins were within normal limits. No real ci ?Se for her diarrhoea was found. She was treated with codeine phosphate, ^Promazine, iron and vitamin C and her general condition improved jj^^derably. She was discharged on the 29th July, 1966, to live with a nephew iti ^"byshire. She was quite happy to go to live with him. She will be seen ?ut patients when she is next in this region. DISCUSSION Before the advent of successful reconstructive aortic surgery, abdominal aortic aneurysm was a condition for which there was no effective therapy. In 1950 Estes reviewed 102 cases of abdominal aortic aneurysms and made a11 effort to outline clearly the natural history of this disease. Since then excision of aneurysms with replacements by homografts and more recently by synthetic materials became widespread.
Pain is the most important symptom of a rupturing abdominal aneurysm-This is accompanied by abdominal discomfort. Significant signs in the diag* nosis of an unruptured abdominal aneurysm include the palpation of a pulsatile, expansile abdominal mass, and curvilinear calcification on abdominal radiography. Intravenous aortagraphy, though used to establish the diagnosis by a few surgeons in the United States, is considered an unnecessary investigation by most vascular surgeons today. An abdominal aneurysm can be easily diagnosed without the aid of an aortogram. Also when the aorta, which may be thinned and contains atheromatous plaques, is punctured in translumbar aortography, there is a danger of rupturing it or dislodging a plaque or thrombus. The differential diagnosis of an abdominal aneurysm includes a pulsatile normal aorta in thin patients or patients with lordotic spines, abdominal masses adjacent to the abdominal aorta, and tortuosity of a normal-sized aorta.
The patient was known to have the abdominal aneurysm almost a yeaf before she was admitted to hospital. Although she was not pressed to have the operation, because of her reluctance, she was undergoing a great risk of rupture. Operation after rupture has occurred leads to a much higher mortality than operation before rupture. De  When a rupture occurs it may be into the retroperitoneum, the peritonea' cavity, or the duodenum. Rupture is followed by collapse, sudden abdomina* pain, rigidity and ileus. The oudook for patients who suffer from untreated aneurysm of the abdominal aorta is poor. A great number die within a yeaf of diagnosis and most are dead within five years.
The patient's blood pressure was 160/90 when examined by the G.P., and 190/90 on admission to hospital. The incidence of hypertension in abdominal aortic aneurysms is well known. Out of 94 patients with abdominal aneurysm^ Estes (1958) found that twenty-five of the sixty-eight males (36.8%) and sixteen of the twenty-six females were hypertensive. For the purpose analysis hypertension was considered to be present if the blood pressure was above 160 systolic or 100 diastolic, expressed in millimetres of mercury-Steinberg and Stein (1966) also produced a similar percentage when they found that 80 of their 200 consecutive cases (40%) were hypertensive. The patient's aneurysm extended from below the level of the renal arteries to the bifurcation of the aorta into the common iliac arteries. This is the common site for an abdominal aortic aneurysm. Of 200 consecutive cases o aortic aneurysms diagnosed by intravenous aortography Steinberg and Stein found 12 patients (6%) with aneurysms above the level of the renal arteries. 36 (18%) the aneurysm was primarily at the bifurcation of the aorta. In aknost 95% of the cases the aneurysm was below the renal arteries.
While many thoracic aneurysms used to be syphilitic in origin the greater Percentage of abdominal aneurysms are atherosclerotic in origin, usually Evolving the lower abdominal aorta as already mentioned. The reason for fois anatomic predilection has never been completely clear but the explanallon of Blakemore deserves careful consideration. He suggested that the e*planation of the development of aneurysm resulting from atherosclerosis ?f the lower abdominal aorta was due to several factors:?
(a) Widespread atherosclerosis tends to involve the entire aorta, including the abdominal segment; (b) the pressure of pulse waves striking the aortic bifurcation and the iliac arteries tends to produce a reverse wave that meets the oncoming next pulse wave. This results in a stress on the aortic wall which is not well supported by sheathing or surrounding tissues at this point; (c) the stress may be aggravated by the fact that the aorta is fixed at the diaphragm and by the iliac fossa. Between these two fixed points the aorta tends to elongate with therosclerosis. It usually deviates to the left. (This occurred in the patient, as seen on the x-ray.) This bending tube tends with further strain to dilate into a fusiform aneurysm. This lack of fixation and the deviation forward also explains why erosion of the spine is rare in abdominal aneurysms as compared with thoracic aneurysms (Blakemore and Voorhees, 1954). Because of the poor general condition of the patient during the operation, T^ing of the aneurysm was performed in place of the favoured procedure ?day of resection and replacement. The replacement can be with a homograft r with a prosthesis of Teflon Dacron, Orion, Vinyon N or other plastic, ^ther types of operation, some only occasionally performed now, include or complete external reinforcement or wrapping with cellophane and i th?r materials. The purpose of wiring of the aneurysm is to produce throm-?sis within the aneurysm, with or without endothermy. , What could one say of the prognosis of this patient? It would be necessary ere to consider several factors. By reason of her age she cannot expect to live Jpf long. The state of her heart is also a factor against her. However, had 116 not had surgical intervention her prognosis would have been even poorer. This patient was first seen by Mr. Peacock at an out-patients clinic if August 1964. He was an insurance superintendent and was then 57 years old-He had a history of four to five years of attacks of a grey film descending over his left eye, partially or completely blocking his sight. The attacks had be^n infrequent at first, having come on every six months or so, but were novV occurring more often and in the previous week he had had two very brief attacks. Two months previously in June, 1964, he had had an epileptiform convulsion lasting five to ten minutes during his sleep. At the time he waS lying on his left side and it was suggested that there might have been occlusion of his left internal carotid artery. His blood pressure after the attack ^aS found by his general practitioner to be 80/50 mm. Hg.
Investigations carried out at the Burden Neurological Institute had shoWjJ (1) E.E.G.: an irregular " delta focus " in the left emporal region. (2) LeP carotid angiogram: Severe carotid stenosis 2 cms. beyond the origin of the internal carotid extending over a distance of 5 cms., with retadation of ^ intracranial circulation rate. The appearances were those of severe atherofl13 There was an excellent collateral supply through the occipital artery to ^ basilar.
Besides the atheromatous block mentioned above it was felt that thefe might possibly have been a stenosis of the innominate artery as there was * systolic bruit over the right carotid, and the blood pressure in the right ^ was 90/60 mm. Hg., whereas on the left side it was 120/80 mm. Hg. It vva5 felt advisable to do an angiogram on the innominate artery by retrogra^ catheterisation of his femoral artery so that a complete picture of the vasculaf supply to the brain could be obtained. It also seemed advisable to do 3 carotid endarterectomy on the left side.
The patient was admitted to the Bristol Royal Infirmary on the 15th Sep' tember, 1964. He had no history of hypertension, tuberculosis or diabetes-He had smoked twenty cigarettes a day for many years. A review of h'5 systems revealed nothing more than was already known.
On examination he was found to be a fit looking middle-aged man. Th&e, was no clubbing of fingers, cyanosis or jaundice. There were no signs ?x anaemia or dehydration.
His pulse was 80/minute and regular. The left radial pulse was a greats volume than the right. The radial pulse was delayed but of normal character- The vessel wall was not palpable. The jugular venous pulse was not raised-The apex beat was not palpable. On auscultation the first and second heafl sounds were heard but were reduced in the aortic area. There were n?

Plate XXVII
The above x-ray of the abdomen taken before the operation shows the curvilinear calcification in the wall of the abdominal aorta. This is seen to the left of the spine with its convexity towards the left. This is the usual direction of deviation of an abdominal aneurysm.

Plate XXVII
The above x-ray of the abdomen taken before the operation shows the curvilinear calcification in the wall of the abdominal aorta. This is seen to the left of the spine with its convexity towards the left. This is the usual direction of deviation of an abdominal aneurysm.
Plate XXVIII This is an x-ray print of the aneurysm showing the steel wiring in the aneurysm. When the aneurysm was seen at the second operation ten days after the wiring it. was no longer pulsatile.
Plate XXVIII This is an x-ray print of the aneurysm showing the steel wiring in the aneurysm. When the aneurysm was seen at the second operation ten days after the wiring it was no longer pulsatile.
Murmurs. There was a systolic thrill and bruit over the right carotid. All the Peripheral pulses were found to be normal. The blood pressure was 80/50 mm. % in the right arm and 130/80 mm. Hg in the left arm. The temperature was 98.2?f.
The trachea was central and there were no palpable neck glands. The chest was barrel-shaped and had a fair degree of expansion, this being greater on the right than on the left. The percussion note was resonant and the breath sounds were vesicular. There were no adventitious sounds. Examination of the central nervous system and the abdomen revealed no abnormality. The ^ndi were normal.
Aortography was carried out by the introduction of a catheter into the right femoral artery by the Seldinger technique. The catheter was passed upwards that its tip lay in the ascending aorta. An injection of 30 c.c. of 85% Hypaque" was given. Films were taken at the rate of four a second for three seconds. The arch of the aorta appeared normal and the origin of the j^ajor vessels appeared normal. The right subclavian artery appeared to be Rocked just beyond its origin and the left vertebral artery was also blocked.
Atheromatous changes were seen in both the common carotid arteries.
On the 26th September, 1964, Mr. Peacock explored the left internal carotid ^"tery. This was done under hypothermia using a left submandibular incision. ^ very adherent mass of glands was found, making it difficult to mobilise the jjtery. However when the artery was exposed it was found to be normal at the beginning of the internal carotid, although there was atheroma present at the bifurcation. As a good pulse was felt in it it was decided not to re-explore the artery further, and it was thought that the narrowing was Probably caused by pressure from without.
The patient developed some wound swelling post-operatively, but this ^ettled on conservative treatment and he was sent home on the 2nd October, 1964.
When seen at a post-operative follow-up clinic a month later he was quite ^ell generally except for a complaint of paresthesia of his right hand. It was j^ot^quite clear whether he had early wasting of the thenar eminence of this . Two months later in January, 1965, he had no symptoms at all. He was r!?ht handed and could play golf. His carotids were equally palpable on each lde. There was a loud bruit over the right carotid and a softer one over the e*t. Examination of his central nervous system showed no abnormality. When seen again in the follow up clinic six months later in July, 1965, he , as well but complained of a pain in the corner of the left eye. He had not ad a pain of this sort since the operation ten months previously.
In January, 1966, there was a recurrence of visual attacks, these being in J*? right eye. They occurred about once a week, and each attack lasted a few ^nutes, causing a partial blindness. (Before 1964 when the patient had had , ttacks in his left eye they had caused complete blindness.) TTiere was also a ?ss of light touch in the 3rd-5th fingers of the left hand.
He was admitted to the Bristol Royal Infirmary on the 6th April, 1966, for two days; again on the 29th April for three days and finally on the 13th May. 1966. On examination he was found to be relatively fit. The blood pressure in the left arm was 120/80 mm. Hg, but was unobtainable in the right. No pulses were palpable in the right arm. All the pulses were normal in the left arm. The right carotid was weaker than the left. There was a bilateral carotid bruit, but more marked on the right. Both femoral pulses were palpable, but the pulses distal to these were not palpable.
Diagnosis: Clinically the patient was thought to have generalised atherosclerosis with a right sided subclavian occlusion and a narrowed right carotid causing the transient blindness in the right eye and the loss of touch in the left hand.
He was investigated by an arch aortogram which revealed several interesting features. The innominate and left common carotid arteries arose as a common trunk from the aortic arch. The left internal carotid artery was blocked just beyond its origin. The left vertebral artery was completely occluded. The right common carotid artery was very narrow. There was a short block in the right subclavian artery of about 1 cm. in length. The right vertebral artery filled retrogradely and the distal part of the right subclavian artery filled from and through an anastomosis around the thyrocervical trunk.
It was felt that his most important symptom was cerebral, and it was decided to remove the partial occlusion from the right common carotid by endarterectomy.
On the 20th May, 1966, Mr. Terblanche exposed the common, internal and external carotid arteries. This was done using surface cooling hypo* thermia carried out by Professor Clutton-Brock. The patient was cooled to 29 ?C. Clamps were applied to the arteries and an incision was made into the internal carotid extending down into the common carotid. Atheroma involving the whole area was found. A sot1 platelet clot was found on the surface of the atheroma at the origin of ths internal carotid. The stripping was technically difficult because of the extensive atheroma extending up and down the carotid vessels.
When the clamps had been on for almost fifteen minutes a local by-pass of polythene tubing was inserted into the lower carotid over a length about 7 cms. Some atheromatous material was also removed from the origin of the external carotid artery-There was now a good back flow from both internal and external carotid arteries. Both the upper flap of atheron)** in the internal carotid and the lower flap of atheroma in the external carotid were sutured down with interrupted silk sutures. Closure of the artery was performed from above downwards with continuous black silk leaving the by-pass in situ until near the end of the anastomosis. When the clamps were removed there was a good flow and pulsation in the arteries. The surface incision was closed with silk, catgut being used deep t0 Post. Ant.

Int.Carotid
Atheroma jf removed Incision Common Carotid lt-The patient was rewarmed and his immediate post-operative course was quite satisfactory. However, late that evening he developed sudden cerebral signs and symptoms. He was noticed to be lethargic and speechless. He was unable to respond to simple orders but reacted to painful stimuli. On examination there generalised hype-tonicity but no localising signs of central nervous system ksions. The pupils were equal and reacted to light. The fundi were normal.
His wound was satisfactory and the pulse rate, blood pressure and respiratory rate were within normal limits. The temperature was 100?F.
Ankle clonus was elicited on both sides. A diagnosis of cerebral oedema was made and the possibility of a cerebrovascular accident was considered.
The following morning (21st May) ankle clonus could be elicited on the left side but no longer on the right. The carotid artery was reexplored by Mr. Peacock and Mr. Terblanche, again under surface cooling hypothermia.
Both the internal and external carotids had retrograde pulsation. There was a region of thrombosis in the common carotid right up to the bifurcation. It was felt that a slight indentation produced by the interrupted sutures used to hold down the proximal flap of atheroma had caused turbulence resulting in thrombosis.
A saphenous vein graft was removed from the right groin. The internal carotid was transected above the suture line. The distal clot was sucked out with great care and a good back flow was obtained. An end-to-end anastomosis of the upper end with the graft was made.
The internal carotid was tied off at the bifurcation and all the blood clot from the common and external carotid was cleared until there was a good back flow and pulsation ?m the distal external carotid. The vein by-pass was anastomised end-to-side * the common carotid. There was now a good flow and pulsation in both e external and internal carotid arteries. ^ *n the post-operative period his condition never really improved and he as kept in the intensive care unit. He was anticoagulated intravenously with By the day after the operation he had a marked left flaccid hemiplegia.
When seen on the second post-operative day by a neurologist he had a flaccid quadriplegia with bilateral extensor plantars and generalised hypotonia. The pupils were fixed and dilated. The femoral vessels revealed severe sclerotic change. There was no swallowing or cough reflex but no other dramatic demonstration of brain-stem nuclear lesion. Nevertheless it was felt that had suffered brain-stem infarction as a result of basilar insufficiency and tha* no further procedure would prove useful. The demonstration of basilar filling from the occipital artery on previous arteriograms tended to suggest h precarious the brain-stem blood supply must have been.
The patient died that afternoon, the 23rd May, 1966. arteries were open. The left common carotid showed a patch of calcific* atheroma just before the bifurcation. The external carotid was normal. The internal carotid was completely occluded by old thrombus one centimetre from the origin. The saphenous vein bypass graft had been working adequately. The brain was heavy and the convolutions were flattened. The cerebellar tonsils had herniated through the foramen magnum. The circle of WiHlS showed mild atheroma only. Both middle cerebral arteries showed consider able atheroma, more marked on the right than on the left. After fixation and serial section of the brain, many small hsemorrhagic infarcts, up to thr# centimetres in diameter, were seen scattered throughout the cerebral hem1' spheres.

DISCUSSION
Three factors usually account for the cerebrovascular insufficiency symp' toms in patients with occlusive disease of the extracranial cerebral arteries These are a decrease in forward flow, a deficiency in collateral supply to brain, and embolisation from ulcerated atheromatous lesions. The severity the symptoms depends on the multiplicity of the occlusive sites and the adequacy of the collateral network.
It is estimated that at least 40% of cerebrovascular accidents are due i0 extracranial vascular disease. Hutchinson and Yates (1961) made a detail^ autopsy study of a hundred patients who had died with a clinical diagnosis o1 cerebral thrombosis. 14 had complete thrombosis of an intracranial arterysix of which were extensions from extra-cranial thrombosis. 58 had significant disease of an external cerebral artery, of which 18 were carotid only, 7 wer6 vertebral only and 33 were carotid and vertebral. The remaining 28 had a wrong initial diagnosis and were mostly cerebral haemorrhage or intracranial tumour. The brain is supplied by four main vessels, the two internal carotid and the two vertebral arteries. When one internal carotid artery is occluded external carotid becomes an important collateral vessel, blood from it reach' ing the circle of Willis mainly by the ophthalmic artery.
. The patient had a very significant though not complete occlusion of his right internal carotid in 1964. He was reported to have an excellent collateral Supply via the occipital artery to the basilar. It will be remembered that an ^astomosis normally exists between the descending branch of the occipital, deep cervical branch of the costocervical (branch of subclavian), and the Vertebral which eventually forms the basilar. . The intracranial circulation rate was retarded by stenosis of the right Eternal carotid. It was still more retarded because the right external carotid *hich, as mentioned above, becomes an important collateral vessel) had to supply to basilar via the occipital. Also the right vertebral was non-functional, ^cause the right sub-clavian was occluded.
. The arch aortogram done just before the first operation showed that the right vertebral artery filled retrogradely and the distal part of the right subclavian artery filled from it. This is the ' subclavian steal' syndrome and may ?ccur in cases of occlusion of the innominate artery or the first part of the subclavian artery with reversal of blood flow in the vertebral artery. Such Patients may present with episodes of vertebro-basilar insufficiency. When the on that side is exercised the vertebral artery acts as a collateral vessel W-t^lat arm. This reduces the blood reaching the brain from the circle of Willis and results in transient cerebral symptoms. The commonest symptoms ^ episodic vertigo, disorders of vision and ' dropping attacks' in which the Patient falls to the ground but remains conscious. Other symptoms include P^esis of 1-4 limbs, transient numbness and paresthesia of the limbs, intense ^ipital headache and buzzing in the ears. The patient presented several of r ese and indeed was considered to have suffered brain-stem infarction as a esult of basilar insufficiency. On clinical grounds alone it is often very difficult to diagnose whether a Patient's symptoms are due to an occlusion of the internal carotid artery. , ue typical symptoms are blindness of the ipsilateral eye and contralateral diplegia with aphasia if the dominant hemisphere is involved. These may be aiisient in which case the likely cause is arterial stenosis. However, the ^Pical clinical syndrome of internal carotid occlusion is not often seen. In a sevries of 200 patients with occlusion of the internal carotid artery, presenting yinptoms included unconsciousness, headache, vomiting, bruit audible to j^tient, deafness, convulsions, dysphagia and severe mental changes apart ?m the more common motor and sensory symptoms, visual disturbances and 'Peech difficulties (Rob, 1965).
Clinically two types of occlusion of the internal carotid are seen; stenosis t Partial occlusion, and complete occlusion. It is often impossible by current int ^ues t0 restore blood flow in complete occlusion if the clot has spread adh cran'a^ Part ?f the carotid or vertebral systems. Here it soon becomes Gnerent and cannot be extracted. It is essential to obtain a satisfactory retro-& ade flow from a patent distal arterial tree if an arterial reconstruction 0cedure is to succeed.
Stenosis on the other hand is easy to deal with surgically. No matter how lQvfre the patient's generalised disease is, it is normal for the internal carotid be unaffected from the stenosis to the circle of Willis. Thus the immediate W?w tract is a good vessel and surgery is of value.
n.a study of 100 patients who had had a major hemiplegia, it was found in more than two-thirds there was a history of previous transient episodes before the major catastrophe (Rob, 1965 In a series of 407 patients with occlusive lesions of the extracranial arteriessurgical treatment was employed in 372 in whom the blood flow to the bran1 was reduced significantly (De Bakey, 1961). They were treated by endartef' ectomy and in many this was combined with patch graft angioplasty. Both the immediate and long term results of operation were extremely gratifying-Normal circulation was restored in all patients with occlusions involving the great vessels arising from the aortic arch and in 96% of patients with incon1' plete occlusive lesions involving the internal carotid and vertebral arteries.
It may be mentioned in passing that surgical procedures designed to increase the efficiency of the collateral circulation in the brain are rarely performed today. These included the formation of a carotid artery to jugular veifj anastomosis, revascularization of the ischemic part of the brain by a collate^1 circulation developed from a graft of temporal muscle implanted in the cerebral cortex, and cervical and perivascular sympathectomy. Most of these were shown by De Souza Pereira to be of little value (De Souza Pereira< 1955)" -a At post mortem, complete occlusion of the patient's left internal carotid was found. The saphenous vein by-pass graft was working adequately. * must be presumed that the patient's episode on the evening after the first operation must have been due to an occlusion of his left carotid and that this was the reason for the failure of both the first and the second operations the right side. The fact that the left vertebral was not shown on the x-ray may be due to a fault in x-ray technique. It was found to be patent at post' mortem. Vascular surgical techniques have advanced considerably and with carefi1' assessment of the indications for surgery, the mortality and morbidity ?j operation can kept at very low levels. The degree of residual neurologic* disability seems to be improved in a fair proportion of surgically treated caseS' Most important of all, prophylactic surgery is of value since very little can done for the patient who has had a major cerebro-vascular accident.